References

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2996 entries

Characterizing the neural substrate of reward with the use of specific brain lesions

Cromwell HC (2021) Characterizing the neural substrate of reward with the use of specific brain lesions. Fakhoury M (Ed.): The Brain Reward System. Neuromethods. 165. Humana, New York, NY doi: 10.1007/978-1-0716-1146-3_3

Summary: This review is focused on experimental lesions and work using the rodent model examining the neural substrates of reward processing. Saporin is listed as a neurotoxin used to target selective neuronal populations with success.

See: Pappas BA et al. Neonatal 192 IgG-saporin lesion of forebrain cholinergic neurons: focus on the life span?. Neurosci Biobehav Rev 27(4):365-376, 2003.

Related Products: 192-IgG-SAP (Cat. #IT-01)

Depletion of C1 neurons attenuates the salt-induced hypertension in unanesthetized rats.

Ribeiro N, Martins Sá RW, Antunes VR (2020) Depletion of C1 neurons attenuates the salt-induced hypertension in unanesthetized rats. Brain Res 1748:147107. doi: 10.1016/j.brainres.2020.147107

Objective: To determine if the ablation of C1 neurons mitigates high blood pressure induced by high-salt intake.

Summary: Data show that hypertension induced by high-salt intake is dependent on C1 neurons.

Usage: Bilateral injections of 2.4 ng/100 nl of Anti-DBH-SAP. The total number of TH+ neurons in the AS region was reduced by 37 ± 13% in the anti-DBH-SAP group when compared to control.

Related Products: Anti-DBH-SAP (Cat. #IT-03)

Sox10 functions as an inducer of the direct conversion of keratinocytes into neural crest cells

Motohashi T, Kawamura N, Watanabe N, Kitagawa D, Goshima N, Kunisada T (2020) Sox10 functions as an inducer of the direct conversion of keratinocytes into neural crest cells. Stem Cells Dev 29(23):1510-1519. doi: 10.1089/scd.2020.0106 PMID: 33040687

Objective: To investigate whether Sox10 functions in the direct conversion of other somatic cells into neural crest cells (NCCs).

Summary: Results demonstrate that Sox10 functions as an inducer of direct conversion into NCCs in cooperation with the transcription factors involved in NCC generation.

Usage: Flow cytometry and cell sorting

Related Products: NGFr (mu p75) Rabbit Polyclonal (Cat. #AB-N01)

Structural and functional consequences of targeted hippocampal gaba neuron ablation by stable substance p-saporin in rats

Chun E (2020) Structural and functional consequences of targeted hippocampal gaba neuron ablation by stable substance p-saporin in rats. Morehouse School of Medicine Thesis.

See: Chun E et al. Targeted hippocampal GABA neuron ablation by Stable Substance P-saporin causes hippocampal sclerosis and chronic epilepsy in rats. Epilepsia 60(5):e52-e57, 2019.

Related Products: SSP-SAP (Cat. #IT-11)

Pseudomonas Exotoxin A based toxins targeting epidermal growth factor receptor for the treatment of prostate cancer

Fischer A, Wolf I, Fuchs H, Masilamani AP, Wolf P (2020) Pseudomonas Exotoxin A based toxins targeting epidermal growth factor receptor for the treatment of prostate cancer. Toxins (Basel) 12(12):753. doi: 10.3390/toxins12120753

Summary: Refers to chimeric murine-human mAb cetuximab bound to Streptavidin-ZAP.

See: Yip WL et al. Targeted Delivery and Enhanced Cytotoxicity of Cetuximab-Saporin by Photochemical Internalization in EGFR-Positive Cancer Cells. Mol Pharm 4(2):241-251, 2007.

Related Products: Streptavidin-ZAP (Cat. #IT-27)

Behavioral, neuromorphological, and neurobiochemical effects induced by omega-3 fatty acids following basal forebrain cholinergic depletion in aged mice

Cutuli D, Landolfo E, Nobili A, De Bartolo P, Sacchetti S, Chirico D, Marini F, Pieroni L, Ronci M, D’Amelio M, D’Amato FR, Farioli-Vecchioli S, Petrosini L (2020) Behavioral, neuromorphological, and neurobiochemical effects induced by omega-3 fatty acids following basal forebrain cholinergic depletion in aged mice. Alzheimers Res Ther 12(1):150. doi: 10.1186/s13195-020-00705-3 PMID: 33198763

Related Products: mu p75-SAP (Cat. #IT-16)

Reversal of object recognition memory deficit in perirhinal cortex-lesioned rats and primates and in rodent models of aging and alzheimer’s diseases.

Masmudi-Martín M, Navarro-Lobato I, López-Aranda MF, Browning PGF, Simón A-M, López-Téllez JF, Jiménez-Recuerda I, Martîn-Montañez E, Pérez-Mediavilla A, Frechilla D, Baxter MG, Khan ZU (2020) Reversal of object recognition memory deficit in perirhinal cortex-lesioned rats and primates and in rodent models of aging and alzheimer’s diseases. Neuroscience 448:287-298. doi: 10.1016/j.neuroscience.2020.08.039

Objective: To determine if Object Recognition Memory (ORM) can be restored.

Summary: Memory-deficient rats were generated by induction of lesions to the perirhinal cortex (PRh) through an injection of OX7-SAP. Expression of regulator of G-protein signaling 14 of 414 amino acids (RGS14414) restored ORM in memory-deficient PRh-lesioned rats and nonhuman primates. This treatment was sufficient for full recovery of ORM in rodent models of aging and Alzheimer’s disease.

Usage: Rats were injected with OX7-SAP (0.9 mg in 1ml) in the PRh of the brain.

Related Products: OX7-SAP (Cat. #IT-02)

Loss of diffuse noxious inhibitory control after traumatic brain injury in rats: A chronic issue

Irvine KA, Sahbaie P, Ferguson AR, Clark JD (2020) Loss of diffuse noxious inhibitory control after traumatic brain injury in rats: A chronic issue. Exp Neurol 333:113428. doi: 10.1016/j.expneurol.2020.113428

Objective: To confirm hypothesis that dysfunctional descending noradrenergic and serotonergic pain control circuits may contribute to the loss of diffuse noxious inhibitory control (DNIC), a critical endogenous pain control mechanism, weeks to months after traumatic brain injury (TBI).

Summary: Results suggest that TBI causes maladaptation of descending nociceptive signaling mechanisms and changes in the function of both adrenergic and serotonergic circuits. Such changes could predispose those with TBI to chronic pain.

Usage: Anti-DBH-SAP (5 μg/5 μl) was injected in the left ventricle. Lesion of the LC resulted in failure of DNIC, an effect that mimics what is observed behaviorally after chronic TBI.

Related Products: Anti-DBH-SAP (Cat. #IT-03)

Noradrenaline signaling in the LPBN mediates amylin’s and salmon calcitonin’s hypophagic effect in male rats.

Boccia L, Le Foll C, Lutz TA (2020) Noradrenaline signaling in the LPBN mediates amylin’s and salmon calcitonin’s hypophagic effect in male rats. FASEB J 34(11):15448-15461. doi: 10.1096/fj.202001456RRR

Objective: To assess the phenotype of amylin activated LPBN (lateral parabrachial nucleus) neurons, especially to confirm the CGRPergic phenotype and to uncover the specific role of NA (noradrenaline) signaling from the AP to the LPBN.

Summary: The present study confirmed the central role of the LPBN in propagating amylin’s and sCT’s hypophagic action, and particularly the importance of AP → LPBN NA signaling in the mediation of this process, through the activation of LPBN (CGRP and non-CGRP) neurons.

Usage: The neuronal pathways used to process the physiological response to amylin were investigated using 50-ng injections of Anti-DBH-SAP (Cat. #IT-03) into the area postrema (AP) or 25 ng into the lateral parabrachial nucleus (Potes et al., 2010).

Related Products: Anti-DBH-SAP (Cat. #IT-03)

Spinal microglia-neuron interactions in chronic pain.

Ho IHT, Chan MTV, Wu WKK, Liu X (2020) Spinal microglia-neuron interactions in chronic pain. J Leukoc Biol 108:1575-1592. doi: 10.1002/JLB.3MR0520-695R

Summary: Spinal microglial activation is initiated shortly and persisted for more than 3 mo after partial sciatic nerve ligation. Intrathecal injection of Mac1-SAP, a saporin-conjugated anti-CD11b antibody to deplete microglia, abolished cold and mechanical allodynia for 2–12 wk after injury,92 supporting the role of activated microglia for chronic pain maintenance.

Related Products: Mac-1-SAP rat (Cat. #IT-33)

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